Understanding the Cardiac Cycle and Wiggers Diagram in Clinical Practice
Core Physiologic Principles
The cardiac cycle, as represented by the Wiggers diagram, is fundamentally a graphical depiction of the pressure-volume relationships that determine ventricular performance, with each cycle characterized by end-diastolic and end-systolic conditions that reflect the interaction between myocardial contractility (inotropy), relaxation (lusitropy), preload, and afterload. 1
The Wiggers diagram displays simultaneous cardiac events across multiple parameters:
- Pressure changes in the left atrium, left ventricle, and aorta that drive blood flow down pressure gradients 2
- Volume changes in the ventricle throughout filling and ejection phases 1
- Valve opening and closing determined by pressure gradients across the atrioventricular and semilunar valves 2
- ECG waves that trigger the mechanical events of each subsequent phase 3
- Heart sounds corresponding to valve closure events 3
Clinical Significance in Cardiac Disease Management
Understanding Systolic vs. Diastolic Dysfunction
The severity and prognosis of heart failure correlate more closely with diastolic filling abnormalities than with ejection fraction alone, making understanding of the cardiac cycle phases critical for diagnosis and management. 4
Systolic dysfunction manifests as:
- Reduced contractility (decreased inotropy) shifting the end-systolic pressure-volume relationship rightward and downward 1
- Decreased stroke volume and cardiac output despite compensatory mechanisms 5
- Coronary artery disease causes approximately two-thirds of systolic dysfunction cases 5
Diastolic dysfunction presents with:
- Impaired ventricular relaxation (decreased lusitropy) causing elevated filling pressures despite preserved ejection fraction 6, 7
- Approximately 20-40% of heart failure patients have preserved systolic function with primary diastolic impairment 6
- Grade 2 diastolic dysfunction carries 39% survival in certain populations, demanding aggressive management 7
The Law of Laplace and Ventricular Remodeling
Wall stress = (Pressure × Radius) / Wall Thickness explains the vicious cycle of heart failure progression visible on pressure-volume loops 5:
- Chamber dilatation increases radius, directly increasing wall stress 5
- Increased wall stress depresses mechanical performance 5
- Spherical remodeling creates regionally variable stress worsening mitral regurgitation 5
- This remodeling precedes symptoms by months to years and continues despite treatment 5
Diagnostic Application
Identifying Structural Abnormalities
Two-dimensional echocardiography with Doppler flow studies is the single most useful diagnostic test for evaluating cardiac cycle abnormalities, as it directly visualizes chamber dimensions, wall motion, valve function, and filling patterns. 6
Key diagnostic considerations:
- Symptoms alone are insufficient for diagnosis; objective evidence of cardiac dysfunction at rest is mandatory 7
- Poor correlation exists between symptom severity and degree of dysfunction 7
- Clinical response to diuretics or nitrates is supportive but not diagnostic without objective assessment 7
Pressure-Volume Loop Analysis
The pressure-volume loop provides external work assessment of the ventricle 1:
- End-diastolic pressure and volume reflect preload and lusitropic state 1
- End-systolic pressure and volume are determined by afterload and inotropic state 1
- Alterations in inotropy and lusitropy produce predictable loop changes facilitating pharmacologic response understanding 1
Management Implications
Systolic Heart Failure
ACE inhibitors or ARBs combined with beta-blockers form the cornerstone of systolic heart failure management, reducing wall stress through pressure reduction and allowing reverse remodeling. 5
Specific mechanisms:
- ACE inhibitors/ARBs reduce pressure (afterload), decreasing wall stress per the Law of Laplace 5
- Beta-blockers reduce sudden death risk and allow reverse remodeling by decreasing pressure and chamber size over time 6, 5
- Diuretics reduce preload and ventricular volume, lowering wall stress 5
- Implantable cardioverter-defibrillator for patients with history of sudden death, ventricular fibrillation, or hemodynamically destabilizing ventricular tachycardia 6
Diastolic Heart Failure
ACE inhibitors or ARBs are cornerstone medications combined with beta-blockers for heart rate control, with target blood pressure <130/80 mmHg. 7
Therapeutic rationale based on cardiac cycle physiology:
- ACE inhibitors/ARBs provide blood pressure control while directly improving ventricular relaxation and promoting regression of left ventricular hypertrophy 7
- Beta-blockers lower heart rate to increase diastolic filling period, allowing more time for ventricular filling in the setting of impaired relaxation 7, 8
- Diuretics are used when fluid overload is present, but titrated carefully to reduce elevated filling pressures without causing excessive preload reduction that compromises cardiac output 7, 8
Special Populations
In elderly patients, aging has a greater impact on diastolic function than systolic performance, with decreased elastic properties, increased myocardial stiffness, and impaired early diastolic relaxation. 8
Age-related changes affecting the cardiac cycle:
- Decreased beta-adrenergic receptor density and peripheral vasodilator capacity exacerbate diastolic dysfunction 8
- Decreased E/A ratio reflects impaired early diastolic relaxation and increased atrial contribution to filling 8
- Morbidity and mortality with preserved ejection fraction may be nearly as profound as with reduced ejection fraction 8
Common Pitfalls to Avoid
Do not rely on ejection fraction alone to assess cardiac function or guide therapy—diastolic filling abnormalities determine prognosis more closely than ejection fraction 4
Do not assume asymptomatic patients have mild disease—patients with very low ejection fractions may be asymptomatic while those with preserved systolic function may have severe disability, reflecting the poorly understood discordance between structural dysfunction and functional impairment 6
Do not overlook the progressive nature of ventricular dysfunction—cardiac remodeling continues after symptom onset and contributes to worsening despite treatment, requiring staged interventions analogous to oncology management 6, 5
In adult congenital heart disease, electro-mechanical coupling requires sophisticated three-dimensional imaging and mapping, as dysrhythmias affect up to 50% of patients and right ventricular assessment poses particular geometric modeling challenges 6